Erythrocytosis Following Testosterone Therapy
Introduction
A rapid increase in awareness of androgen deficiency has led to substantial increases in prescribing of testosterone therapy (TTh), with the benefits of improvements in mood, libido, bone density, muscle mass, body composition, energy and cognition. However, TTh may be limited by its side effects, particularly erythrocytosis. This review examines the literature regarding testosterone-induced erythrocytosis and polycythemia.
Aim
To review the available literature on testosterone-induced erythrocytosis, discuss possible mechanisms for pathophysiology, determine the significance of formulation, and elucidate the potential thromboembolic risk.
Methods
A literature review was performed using PubMed for articles addressing TTh, erythrocytosis, and polycythemia.
Main Outcome Measures
Mechanism, pharmacologic contribution, and risk of testosterone induced erythrocytosis.
Results
For men undergoing TTh, the risk of developing erythrocytosis compared to controls is well established, with short acting injectable formulations having the highest associated incidence. Potential mechanisms explaining the relationship between TTh and erythrocytosis include the role of hepcidin, iron sequestration and turnover, erythropoietin production, bone marrow stimulation, and genetic factors. High blood viscosity increases the risk for potential vascular complications involving the coronary, cerebrovascular, and peripheral vascular circulation, though there is limited evidence supporting a relationship between TTh and vascular complications.
Conclusions
Short acting injectable testosterone is associated with greater risk of erythrocytosis when compared with other formulations. The mechanism of the pathophysiology and its role on thromboembolic events remains unclear, though few data support an increased risk of CV events resulting from testosterone-induced erythrocytosis.
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